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G Morpurgo

Publications and source records attributed to G Morpurgo.

At least 19 recordsLinked to original sources
PubMed1999

Starvation in yeast increases non-adaptive mutation.

The frequency of reversion in a histidine-requiring mutant of Saccharomyces cerevisiae increases about ten-fold in stationary cells during histidine starvation. Histidine starvation enhances a similar frequency of reversion in a tryptophan-requiring mutant. Starvation, therefore, enhances mutation frequencies in a non-adaptive manner. The base analogue 6-N-hydroxylaminopurine (HAP) added prior to plating on medium with limited histidine strongly increases reversion of the histidine mutant. HAP-induced reversion increases further in stationary starving cells with the same kinetics as that which increases spontaneous reversion. Adding HAP to the stationary starving cells does not produce any effect.

Adenine↗
PubMed1998

The uvsC and uvsE genes of Aspergillus nidulans are not required for the mutagenic repair of UV damage.

The uvsC gene of Aspergillus nidulans is a homolog of the RAD51 gene of Saccharomyces cerevisiae. However, with respect to its effects on UV mutagenesis, it differs from the yeast gene, since it seems to be required for UV mutagenesis; however, this conclusion is based only on data from resting conidia. To further clarify the functional role of the uvsC gene, we tested the UV mutability of strains bearing a uvsC mutation in resting as well as in germinating conidia, by the p-fluorophenyl-alanine resistance test. We also evaluated the mutability of the uvsE mutant which belongs to the same epistatic group. Our results show that the uvsC and uvsE genes do not have a significant role in the mutagenic UV-repair pathway.

Aspergillus nidulans↗
PubMed1997

6-N-hydroxylaminopurine (HAP)-induced accumulation of variability in haploid and diploid strains of Aspergillus nidulans.

Haploid and diploid strains of Aspergillus nidulans have been repeatedly treated with the strong mutagen 6-N-hydroxylaminopurine (HAP) which causes only base substitutions. An enormous amount of variability may be rapidly accumulated in haploid or diploid strains of A. nidulans. In particular, in the diploids the analysis of the results shows that after 12 cycles of treatment the conidia differ from each other for about ten recessive lethals and therefore probably for several hundreds of mutations. The viability of the heterozygous multiply mutant diploids is not appreciably different from that of untreated controls. In the diploid strains the accumulated variability was very high. The treatment of a haploid strain during vegetative growth also caused a strong accumulation of mutations, even though deleterious, because they can be maintained in the heterokaryotic condition.

Adenine↗
PubMed1997

The base analog 6-N-hydroxylaminopurine (HAP) mutagenesis is dependent on the integrity of the uvsE, uvsF and uvsB genes in Aspergillus nidulans.

Most of the available data in lower eukaryotes are consistent with the idea that base analogs-induced mutagenesis is due to the mis-pairing properties of these compounds, which, in turn, is due to a shift in the tautomeric equilibrium of the molecule. A tautomeric shift may in fact lead to mismatches which, at least in Escherichia coli, can be repaired by genes involved in the post-replicative mismatch repair whose activity is necessary to control spontaneous mutagenesis. In filamentous fungi, such as Aspergillus nidulans, nothing is known about the repair of base pairing mistakes after base analogs treatment. For this reason, we have decided to screen UV-sensitive Aspergillus nidulans mutants for their mutagenic response to 6-N-hydroxylaminopurine (HAP). We have shown that three mutations (uvsB, uvsC and uvsE), which enhance the UV-sensitivity of germinating conidia, cause a lower mutagenic response to HAP. On the other hand, the uvsH mutation, has no effect on HAP-induced mutagenesis.

Adenine↗
PubMed1994

The genetic activity of 6-N-hydroxylaminopurine in Aspergillus nidulans.

The activity of a base analog (6-N-hydroxylaminopurine, HAP) has been tested on Aspergillus nidulans. In germinating haploid conidia HAP is a strong mutagen, while it does not have any activity in resting conidia. Moreover, HAP does not increase the frequency of recombination in germinating conidia. The mutagenic activity of this base analog has also been tested in diploid conidia of A. nidulans; in fact, it has been shown (Pavlov et al., 1991) that the HAP-induced frequency of heteroallelic recessive mutations in diploid cells of the yeast S. cerevisiae is higher than expected. In A. nidulans, we did not observe any increase in the frequency of recessive homozygous fpaA/fpaA (p-fluorophenylalanine-resistant) mutants over the expected one, which has been calculated on the basis of the observed mutation frequency in the haploid strain.

Adenine↗
PubMed1991

Protection against malaria morbidity: near-fixation of the alpha-thalassemia gene in a Nepalese population.

We have previously reported that the Tharu people of the Terai region in southern Nepal have an incidence of malaria about sevenfold lower than that of synpatric non-Tharu people. In order to find out whether this marked resistance against malaria has a genetic basis, we have now determined in these populations the prevalence of candidate protective genes and have performed in-vitro cultures of Plasmodium falciparum in both Tharu and non-Tharu red cells. We have found significant but relatively low and variable frequencies of beta-thal, beta S, G6PD (-), and Duffy (a-b-) in different parts of the Terai region. The average in-vitro rate of invasion and of parasite multiplication did not differ significantly in red cells from Tharus versus those from non-Tharu controls. By contrast, the frequency of alpha-thalassemia is uniformly high in Tharus, with the majority of them having the homozygous alpha-/alpha-genotype and an overall alpha-thal gene (alpha-) frequency of .8. We suggest that holoendemic malaria has caused preferential survival of subjects with alpha-thal and that this genetic factor has enabled the Tharus as a population to survive for centuries in a malaria-holoendemic area. From our data we estimate that the alpha-thal homozygous state decreases morbidity from malaria by about 10-fold. This is an example of selection evolution toward fixation of an otherwise abnormal gene.

Animals↗
PubMed1990

p-fluoro-phenylalanine resistance in Aspergillus nidulans diploid cells: evidence that dominant, lethal mutations are involved.

An unexpectedly large number of p-fluoro-phenylalanine (FPA)-resistant mutants have been recovered after UV-irradiation of wild type diploid conidia of Aspergillus nidulans. At least five different classes of mutants, possibly corresponding to five different loci, have been identified. Two of them may be the dominant loci which have already been described but the others (a minimum of three loci) are completely different. Mutations in these loci confer high level FPA resistance in the heterozygous diploids, being lethal in the haploids; one mutation has been preliminarily mapped to chromosome I and another to chromosome III.

Aspergillus nidulans↗
PubMed1990

Frequency of spontaneous and induced recessive mutations in a diploid strain of Aspergillus nidulans.

The spontaneous and UV-induced frequencies of recessive mutations have been studied in a diploid strain of Aspergillus nidulans, by the p-fluoro-phenylalanine (FPA) and 8-azaguanine (8-AZA) resistance tests, on either resting or germinating conidia. Observed frequencies are in the order of magnitude of those expected, which have been calculated considering the observed mutation frequencies in the haploid strain as well as the mitotic recombination frequencies. We also review some papers which claim to have found higher rates of recessive mutations in mammalian cell lines; in some cases no really higher rates are evident and the authors' conclusions often rest on misinterpretation of their own data.

Aspergillus nidulans↗
PubMed1988

An uvsB mutant of Aspergillus nidulans with high variable spontaneous mutation and intergenic mitotic recombination frequencies.

An UV-sensitive mutant has been isolated with a new technique which allows isolation of UV-sensitive and UV-non-mutable mutants in Aspergillus nidulans. This mutant is an allele of the known uvsB gene but shows some features not previously described in the alleles so far isolated. Its more important characteristics are: (1) Frequency of mitotic intergenic recombination is strongly increased in uvs/uvs diploids and it is highly variable in different clones: it varies from a minimum of 40-fold to a maximum of about 1000-fold in comparison with uvs+/uvs+ strains. (2) The frequency of mitotic intergenic recombination is increased also in the heterozygous diploids. (3) The frequency of spontaneous mutation is higher and highly variable in different subclones: it may be increased up to 1000-fold.

Aspergillus nidulans↗